Diabetes is a chronic systemic disease characterized by disorders in metabolism of insulin, carbohydrates, fats and proteins and in the structure and function of blood vessels. The primary symptom of acute diabetes is hyperglycemia, often accompanied by diabetes, the presence in urine of large amounts of glucose, and polyuria, the excretion of large volumes of urine. Additional symptoms including degeneration of the walls of blood vessels arise in chronic or long standing diabetes. Although many different human organs are affected by these vascular changes, the eyes and kidneys appear to be the most susceptible. As such, long-standing diabetes mellitus, even when treated with insulin, is a leading cause of blindness.
There are three recognized types of diabetes mellitus. Type I diabetes or insulin dependent diabetes mellitus (IDDM) is typically of juvenile onset; ketosis develops early in life with much more severe symptoms and has a near-certain prospect of later vascular involvement. Control of Type I diabetes is difficult and requires exogenous insulin administration. Type II diabetes or non-insulin dependent diabetes mellitus (NIDDM) is ketosis-resistant, generally develops later in life, is milder and has a more gradual onset. Gestational diabetes is related to type II diabetes and associated with an increased risk of later development of that disease. Type III diabetes is malnutrition-related diabetes.
Insulin (hereinafter, referred to as “INS”) is a hormone secreted from particular β cells of the pancreas that regulates carbohydrate and fat metabolism in the body by triggering cells to absorb glucose. Human recombinant polypeptide A and B chains of mature INS or pINS were synthesized in E. coli as the result of cloning rat and human INS cDNA. To date, INS therapy has been solely focused on reducing blood glucose levels.
Therefore, it is necessary to provide an unknown immunological function of INS.